Imidacloprid

A Neonicotinoid

Alan YanahanCPSC 270, 2009

History Late 1970s: chemists at Shell

Chemical Company laid the groundwork for the future synthesis of imidacloprid through their investigations of potential insecticides

1984: chemists as Nikon Bayer Agrochem create imidacloprid First neonicotinoid insecticide registered

for use

Imidacloprid

Compared to nicotine Less human toxicity and greater effectiveness against insects

Systemic insecticide Used on a wide variety

of fruit and vegetable crops

Used in termite control and in flea control on pets

How Does Imidacloprid Work?

Have to understand the nervous system first

The Nervous System Nerve cells

transmit messages from one another by means of electrical impulses (action potentials)

The axon carries the message away from one nerve cell to the dendrites of another nerve cell

The Nervous System Between the axon

and dendrite is a gap referred to as the synapse

In order for the electrical message to cross the synapse, it must be converted into a chemical message

The Nervous System When an electrical impulse

reaches the end of an axon, it leads to the release of chemicals called neurotransmitters

These neurotransmitters bind with receptors on the dendrites of neighboring nerve cells to cause the generation of another electrical impulse

Enzymes break down neurotransmitters to prevent nerve cells from repeatedly firing

What Does This Look Like?

Ca2+

Ca2+

Ca2+

Na+Na+

Na+

Axon of pre-synaptic cell receives action potential and voltage gated Ca2+ channel opens

Calcium ions (Ca2+) enter axon

Voltage gated Ca2+ channel closes

Vesicle releases acetylcholine (neurotransmitter) into nerve synapse

Acetylcholine

Vesicle

Acetylcholine binds with receptor (nicotinic acetylcholine receptor)

Nicotinic acetylcholine receptor opens

Sodium ions (Na+) enter the dendrite and cause an action potential in post-synaptic cell

Acetylcholine is released from nicotinic acetylcholine receptor

Nicotinic acetylcholine receptor closes

Acetylcholine binds with the enzyme acetylcholinesterase

Choline is released

Acetate is released

When Imidacloprid is Present in the Synapse Imidacloprid mimics the molecular

shape of the neurotransmitter acetylcholine Acts on various nicotinic acetylcholine

receptors to cause nerves to fire Is not recognized by the enzyme

acetylcholinesterase Leads to tremors, convulsion, and

death in insects

What Does This Look Like?

Nicotinic acetylcholine receptor opens

Acetylcholine is released from nicotinic acetylcholine receptor

Nicotinic acetylcholine receptor closes

Acetylcholine binds with the enzyme acetylcholinesterase

Choline is released

Acetate is released

Ca2+

Ca2+

Ca2+

Na+Na+

Na+

Acetylcholine

Imidacloprid binds with the nicotinic acetylcholine receptor

Sodium ions (Na+) enter the dendrite to produce another action potential

Na+

Na+

Na+

Sources Kreiger, Robert I. Handbook of Pesticide

Toxicology 2nd Edition: Agents. Sheets, Larry P. Chapter 54—Imidacloprid: A Neonicotinoid Insecticide. San Diego: Academic Press, 2001

Silverthorn, Dee Unglaub. Human Physiology An Integrated Approach 4th Edition. San Francisco: Pearson Education Inc., 2007.